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The characteristics of coronary artery calcium responsible for vulnerable plaque remain incompletely elucidated. We used optical coherence tomography to investigate the characteristics of coronary calcium in acute myocardial infarction (AMI), unstable angina pectoris (UAP), and stable angina pectoris (SAP). We evaluated calcium deposits in the culprit lesions (30-mm segment) using optical coherence tomography in 187 patients with AMI (n = 44), UAP (n = 73), or SAP (n = 70). The arc, area, and length of calcium were significantly smaller in those with AMI and UAP than in those with SAP (p <0.001). The number of spotty calcium deposits (with an arc of <90°) per patient was significantly larger in the AMI and UAP groups than in the SAP group (p <0.001). The number of large calcium deposits (with an arc of >90°) per patient was significantly lower in the AMI and UAP groups than in the SAP group (p <0.001). The minimum distance between the inner edge of the calcium and the luminal surface was significantly shorter in the AMI and UAP groups than in the SAP group (p <0.001). Plaque rupture frequency correlated positively with the number of spotty calcium deposits (r = 0.479, p <0.001) and inversely with the number of large calcium deposits (r = −0.219, p = 0.003). In conclusion, calcium was very spotty and more superficial in the culprit lesions of AMI and UAP. These characteristics of calcium might play an important role in the pathogenesis of plaque vulnerability.

Neointima inside the bare-metal stents (BMSs) can transform into atherosclerotic tissue during an extended follow-up because of a persistent inflammatory reaction to the metal. We sought to investigate whether strut thickness may impact on the atherosclerotic change in neointima 4 years or more after BMS implantation using optical coherence tomography. Forty-six stented lesions of 41 patients with BMS ≥4 years after implantation who underwent optical coherence tomography were enrolled in the study. The strut was defined as thin when less than 100 μm and thick when ≥100 μm. According to these criteria, stents were divided into 2 groups (thin strut n = 19, thick strut n = 27). Neointimal tissue was categorized into normal neointima, characterized by a signal-rich band without signal attenuation, or lipid-laden intima, with marked signal attenuation and a diffuse border. Intimal disruption, thrombus, and neovascularization were also evaluated. The mean period after implantation was 98.2 ± 25.8 months in the thin-strut group and 91.1 ± 22.8 months in the thick-strut group (P = .330). Lipid-laden intima (70% vs 32%, P = .016), thin-cap fibroatheroma–like intima (59% vs 16%, P = .0056), and intimal disruption (48% vs 16%, P = .031) were observed more frequently in the thick-strut group than in the thin-strut group, but no significant difference was observed in the frequency of thrombus. Although peristrut neovascularization was a common finding in both groups (thick vs thin 81% vs 79%, P = 1.000), the frequency of intraintima neovascularization tended to be higher in the thick-strut group (67% vs 42%, P = .135). A thinner strut thickness may have favorable effects on neointimal atherosclerotic changes after BMS implantation.

The current guideline recommends lowering low-density lipoprotein cholesterol (LDL-C) for the primary management of dyslipidemia in patients at high-risk of cardiovascular events. Patients who have achieved LDL-C levels below the recommended targets may still experience cardiovascular events, suggesting additional therapeutic targets beyond LDL-C. The aim of this study was to investigate whether high-density lipoprotein cholesterol (HDL-C) levels had an impact on plaque stabilization in patients with acute coronary syndrome (ACS). This study consisted of 90 ACS patients with untreated dyslipidemia. In optical coherence tomography (OCT) analysis, a plaque with fibrous cap thickness ≦160 μm was defined as a high-risk plaque. We registered one high-risk plaque per one patient by baseline OCT imaging, and then administrated high-intensity statin. Based on the follow-up OCT results, patients whose registered plaque was no longer high-risk plaque were classified into a responder group and the remains into a non-responder group. No differences were observed in the baseline LDL-C and HDL-C levels between the two groups. Reduction of LDL-C levels (δ LDL-C: -53 ± 21 mg/dL vs. -42 ± 29 mg/dL, p = 0.036) and increase of HDL-C levels (δ HDL-C: 2.5 ± 5.9 mg/dL vs. -0.3 ± 6.7 mg/dL, p = 0.039) were greater in the responder group. On multivariate logistic regression analysis, δ LDL-C levels (OR: 0.956, 95% CI: 0.921-0.993; p = 0.020) and δ HDL-C levels (OR: 1.143; 95% CI: 1.005-1.300, p = 0.041) were independent contributors for plaque stabilization. Increase of HDL-C levels is associated with plaque stabilization in patients with ACS. HDL-C could be a therapeutic target for residual risk management.

Background Even in the current drug-eluting stent era, revascularization for coronary stenosis with fractional flow reserve (FFR) between 0.75 and 0.80, the so-called “gray zone,” is a matter of debate. Previous studies have reported conflicting results regarding outcomes of revascularization versus deferral for coronary stenosis when FFR values are in the gray zone, but these studies have had differing designs and populations. We therefore will investigate whether medical therapy plus percutaneous coronary intervention (PCI) is superior to medical therapy alone in reducing major cardiovascular events in patients presenting with coronary stenosis with gray zone FFR values. Methods/design This is a prospective, multicenter, open-label, parallel group, randomized, controlled, superiority study. A total of 410 eligible participants will be recruited and randomized to either the medical therapy plus PCI group or the medical therapy alone group. The primary endpoint is 1-year major adverse cardiac events (MACEs), defined as a combined endpoint of all-cause death, nonfatal myocardial infarction (MI), or unplanned target vessel revascularization (TVR). Secondary endpoints include MACE at 2 and 5 years. Moreover, each individual component of the primary endpoint, cardiovascular death, target vessel-related and non-target vessel-related MI, all MI, clinically driven TVR or non-TVR, all revascularization, stent thrombosis, and angina symptom status will be evaluated at 1, 2, and 5 years. Discussion This is the first prospective, multicenter, randomized, controlled study to investigate the superiority of medical therapy plus PCI over medical therapy by itself in reducing major cardiovascular events in patients presenting with coronary stenosis with “gray zone” FFR values. The results will help interventional cardiologists in making revascularization decisions regarding coronary stenosis with gray zone FFR values. Trial registration University Hospital Medical Information Network Clinical Trials Registry, UMIN000031526 . Registered on 1 March 2018.

A 47-year-old woman was hospitalized for syncope. An electrocardiogram showed complete right bundle branch block and T-wave inversion in leads III, aVF, and V2–4. Cardiac catheterization was performed since the echocardiogram demonstrated the existence of a left ventricular apical aneurysm and apical thrombus. Coronary angiography revealed normal coronary arteries. An endomyocardial biopsied specimen from the right ventricular apical wall demonstrated typical noncaseating granulomas with giant cells. There was no evidence suggesting the involvement of other systemic organs. The patient was diagnosed as having cardiac sarcoidosis. Cardiac sarcoidosis should be considered within a spectrum of diseases that cause left ventricular apical aneurysm.

Background: Even in the current drug-eluting stent era, revascularization for coronary stenosis with fractional flow reserve (FFR) between 0.75 and 0.80, the so-called “gray zone”, is a matter of debate. Previous studies have reported conflicting results regarding outcomes of revascularization vs. deferral for coronary stenosis when FFR values in the gray zone, but have had differing study designs and populations. We therefore investigate whether medical therapy plus percutaneous coronary intervention (PCI) is superior to medical therapy alone in reducing major cardiovascular events in patients presenting coronary stenosis with gray-zone FFR values. Methods: This is a prospective, multicenter, open-label, parallel group, randomized, controlled, superiority study. A total of 410 eligible participants will be recruited and randomized to either the medical therapy plus PCI or the medical therapy alone group. The primary endpoint is one-year major adverse cardiac event (MACE), defined as a combined endpoint of all-cause death, non-fatal myocardial infarction (MI), or unplanned target vessel revascularization (TVR). Secondary endpoints include MACE at 2 and 5 years. Moreover, each individual component of the primary endpoint, cardiovascular death, target vessel-related and non-target vessel-related MI, all MI, clinically-driven TVR or non-TVR, all revascularization, stent thrombosis, and angina symptom status will be evaluated at 1, 2, and 5 years. Discussion: This is the first prospective, multicenter, randomized, controlled study to investigate the superiority of medical therapy plus PCI over medical therapy by itself in reducing major cardiovascular events in patients presenting coronary stenosis with “gray-zone” FFR values. The results will help interventional cardiologists in making revascularization decisions regarding coronary stenosis with gray-zone FFR values. Trial registration: University Hospital Medical Information Network Clinical Trials Registry, ID: UMIN000031526. Registered on 1 March 2018. Key Words: Coronary physiology, fractional flow reserve, medical therapy, percutaneous coronary intervention

We recently isolated a Krüppel-like zinc-finger transcription factor 5 (KLF5; also known as BTEB2 and IKLF), which is markedly induced in activated vascular smooth-muscle cells and fibroblasts. Here we describe our analysis of the in vivo function of KLF5 using heterozygous KLF5-knockout mice ( Klf5 +/− ). In response to external stress, Klf5 +/− mice showed diminished levels of arterial-wall thickening, angiogenesis, cardiac hypertrophy and interstitial fibrosis. Also, angiotensin II induced expression of KLF5, which in turn activated platelet-derived growth factor-A (PDGF-A) and transforming growth factor-β (TGF-β) expression. In addition, we determined that KLF5 interacted with the retinoic-acid receptor (RAR), that synthetic RAR ligands modulated KLF5 transcriptional activity, and that in vivo administration of RAR ligands affected stress responses in the cardiovascular system in a KLF5-dependent manner. KLF5 thus seems to be a key element linking external stress and cardiovascular remodeling.

Although the plasma B-type natriuretic peptide (BNP) level is a marker of heart failure, it is unclear whether BNP per se plays a pivotal role for pathogenic mechanisms underlying the development of ischemic heart disease (IHD). In this study, we retrospectively examined the plasma BNP levels in stable patients with IHD and compared to stable patients with cardiovascular diseases other than IHD. The study population was 2088 patients (1698 males and 390 females) who were admitted to our hospital due to IHD (n = 1,661) and non-IHD (n = 427) and underwent cardiac catheterization. Measurements of the hemodynamic parameters and blood sampling were performed. The plasma BNP levels were significantly lower in the IHD group than in the non-IHD group (p<0.001). The multiple regression analysis examining the logBNP values showed that age, a male gender, low left ventricular ejection fraction, low body mass index, serum creatinine, atrial fibrillation and IHD per se were significant explanatory variables. When the total study population was divided according to gender, the plasma BNP levels were found to be significantly lower in the IHD group than in the non-IHD group among males (p<0.001), but not females (p = NS). Furthermore, a multiple logistic regression analysis of IHD showed the logBNP value to be a significant explanatory variable in males (regression coefficient: -0.669, p<0.001), but not females (p = NS). The plasma BNP levels were relatively low in stable patients with IHD compared with those observed in stable patients with non-IHD; this tendency was evident in males. Perhaps, the low reactivity of BNP is causally associated with IHD in males. We hope that this study will serve as a test of future prospective studies.